An understanding of the mechanisms that underlie primary palate development is necessary for further progress to be made in research related to malformations such as cleft lip and palate. We have employed the chick embryo as a model system because it permitted analysis of both cell proliferation and cell migration. From our past studies we have determined that an orderly, sequential pattern of decline in rates of cell proliferation produces region-specific differences in growth rates throughout the primary palate. This pattern of decline is closely associated with the appearance of subpopulations of cells which exit from rapidly proliferating pools and appear to be quiescent. Complementary cell migration studies have revealed that major translocations of mesenchyme and associated epithelia occur during facial process formation. The findings from this project are currently being extended in other studies to analyze the pathogenesis of oro-facial clefting in mammalian embryos. Further efforts will be directed toward determining the factors responsible for the emergence and stability of quiescent cell populations by: 1) characterizing the cell cycle block of quiescent cell populations; 2) analyzing the pattern of vascularization during primary palate formation; 3) analyzing the pattern of communication of mesenchymal cells in the primary palate and 4) relating these patterns to the appearance of quiescent cell populations. Double-label two-emulsion autoradiography, transmission electron microscopy, and microangiography will be employed in these studies. Morphogenetic movements (including cell recruitment) will be analyzed to delineate the changing domains and interrelationships of each of the facial primordia. An implant labelling technique utilizing sable hair probes as a carrier for a 3H-thymidine marker will be used to determine the precise location of the territories of each of the facial primordia and the primordia and the contribution of each to fully developed structures.